Limits...
Chlamydia pneumoniae infection of the central nervous system worsens experimental allergic encephalitis.

Du C, Yao SY, Ljunggren-Rose A, Sriram S - J. Exp. Med. (2002)

Bottom Line: Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis.Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS.These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

ABSTRACT
Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

Show MeSH

Related in: MedlinePlus

Immunohistochemical detection of chlamydial antigens in the spinal cords of mice with EAE. (a) Presence of chlamydial antigens in lung tissue from Balb/c mice, infected intranasally with C. pneumoniae and stained with Mab 807. (b) Representative areas of perivascular infiltration/inflammation in C. trachomatis-infected mice with EAE, showing no staining with Mab 807. (c and d) Representative areas of perivascular lymphocytic inflammation of C. pneumoniae-infected mice with EAE, indicating staining with Mab 807 (arrows).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2196067&req=5

fig3: Immunohistochemical detection of chlamydial antigens in the spinal cords of mice with EAE. (a) Presence of chlamydial antigens in lung tissue from Balb/c mice, infected intranasally with C. pneumoniae and stained with Mab 807. (b) Representative areas of perivascular infiltration/inflammation in C. trachomatis-infected mice with EAE, showing no staining with Mab 807. (c and d) Representative areas of perivascular lymphocytic inflammation of C. pneumoniae-infected mice with EAE, indicating staining with Mab 807 (arrows).

Mentions: To directly demonstrate the presence of C. pneumoniae in the CNS, spinal cords were obtained from mice which were infected with C. pneumoniae and induced to develop EAE. Spinal cords were stained with anti-chlamydial antibodies using standard immunohistochemical techniques. Intracellular staining of perivascular mononuclear and CNS parenchymal cells with anti-chlamydial antibodies was seen in at least one section of all four mice examined (Fig. 3, c and d) . No staining of elementary bodies were seen in mice immunized with MSCH and inoculated with C. trachomatis (Fig. 3 b). The monoclonal antibody 807 recognizes LPS and MOMP antigens of both C. trachomatis and C. pneumoniae. No staining of chlamydial antigens was seen in mice with EAE and infected with C. pneumoniae after incubation with an irrelevant control antibody (anti–E. coli LPS antibody, unpublished data). These results corroborate our observations on RT-PCR and offer direct evidence of infection by C. pneumoniae of the CNS.


Chlamydia pneumoniae infection of the central nervous system worsens experimental allergic encephalitis.

Du C, Yao SY, Ljunggren-Rose A, Sriram S - J. Exp. Med. (2002)

Immunohistochemical detection of chlamydial antigens in the spinal cords of mice with EAE. (a) Presence of chlamydial antigens in lung tissue from Balb/c mice, infected intranasally with C. pneumoniae and stained with Mab 807. (b) Representative areas of perivascular infiltration/inflammation in C. trachomatis-infected mice with EAE, showing no staining with Mab 807. (c and d) Representative areas of perivascular lymphocytic inflammation of C. pneumoniae-infected mice with EAE, indicating staining with Mab 807 (arrows).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196067&req=5

fig3: Immunohistochemical detection of chlamydial antigens in the spinal cords of mice with EAE. (a) Presence of chlamydial antigens in lung tissue from Balb/c mice, infected intranasally with C. pneumoniae and stained with Mab 807. (b) Representative areas of perivascular infiltration/inflammation in C. trachomatis-infected mice with EAE, showing no staining with Mab 807. (c and d) Representative areas of perivascular lymphocytic inflammation of C. pneumoniae-infected mice with EAE, indicating staining with Mab 807 (arrows).
Mentions: To directly demonstrate the presence of C. pneumoniae in the CNS, spinal cords were obtained from mice which were infected with C. pneumoniae and induced to develop EAE. Spinal cords were stained with anti-chlamydial antibodies using standard immunohistochemical techniques. Intracellular staining of perivascular mononuclear and CNS parenchymal cells with anti-chlamydial antibodies was seen in at least one section of all four mice examined (Fig. 3, c and d) . No staining of elementary bodies were seen in mice immunized with MSCH and inoculated with C. trachomatis (Fig. 3 b). The monoclonal antibody 807 recognizes LPS and MOMP antigens of both C. trachomatis and C. pneumoniae. No staining of chlamydial antigens was seen in mice with EAE and infected with C. pneumoniae after incubation with an irrelevant control antibody (anti–E. coli LPS antibody, unpublished data). These results corroborate our observations on RT-PCR and offer direct evidence of infection by C. pneumoniae of the CNS.

Bottom Line: Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis.Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS.These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

ABSTRACT
Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

Show MeSH
Related in: MedlinePlus